Ischemia-Induced Release of (3H) norepinephrine from Rat Cerebral Cortex Slices
Journal of the Korean Neurological Association
; : 177-186, 1995.
Artigo
em Coreano
| WPRIM (Pacífico Ocidental)
| ID: wpr-98443
Biblioteca responsável:
WPRO
ABSTRACT
OBJECTIVE & BACKGROUND:
It has been shown that cerebral ischemia alters brain monoamine metabolism. In an attempt to elucidate the. Mechanism for ischen-iiainduced release of neurotransmitters in vitro, we examined the ischemia-induced release of (3H) norepinephrine (NE) from cerebral cortex of the rat.RESULTS:
Ischemia, deprivation of oxygen and glucose, induced significant (about 12% of total tissue content) release of (3H)NE from cerebral cortex in vitro. This ischemia-induced release of (3H)NE from cerebral cortex was significantly attenuated by 1 mM TTX (tetrodotoxin), 1. 2 mM Mg2+, 10 mM MK-801, 10 mM ketamine, NMDA receptor antagonist, 30 mM DNQX, a kainate/AMPA receptor antagonist, or a 30 mM carbetapentane, an inhibitor of glutarnate release Dantrolene(30 mM) and ryanodine (100 nM), inhibitors of intraceuular Ca2+ release, flunarizine(5 mM) and w-conotoxin (100 nM), inhibitors of N-type Ca2+ channels, significantly attenuated the ischeniiainduced release of (3H)NF, but verapamil (5mM), an inhibitor of L-type Ca2+ channels, did not. Nisoxetine(100 nM), a relative NE transporter blocker, significantly inhibited the ischemia-induced release of (3H) NE. Removal of Ca2+ from the incubation media potently increased ischemia-induced (3H)NE release.CONCLUSION:
These results suggest that ischemia-evoked release of norepienphrine was caused by release of glutamate via activation of NMDA and non-NMDA receptors, and that Ca2+-dependent and -independent release processes are underlying in this phenomenon.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Oxigênio
/
Rianodina
/
Encéfalo
/
Verapamil
/
Norepinefrina
/
Córtex Cerebral
/
Isquemia Encefálica
/
Maleato de Dizocilpina
/
N-Metilaspartato
/
Neurotransmissores
Limite:
Animais
Idioma:
Coreano
Revista:
Journal of the Korean Neurological Association
Ano de publicação:
1995
Tipo de documento:
Artigo